Immune complexes glomerulonephritis

Type III Reactions These reactions involve the presence of antigen-antibody complexes, particularly those formed as a result of the production of autoantibodies. These complexes deposit in various tissues and involve inflammatory cells as well as complement, resulting in tissue damage due to the production of proteolytic enzymes by polymorphonuclear leukocytes and macrophages. A number of autoimmune diseases result from these reactions. Some clinical examples include systemic lupus erythematosus, rheumatoid arthritis, immune complex glomerulonephritis, Arthus reaction and serum sickness. 

Nephrotic syndrome and immune complex glomerulonephritis have been attributed to chlorpropamide (119). 

Appel GB, D Agati V, Bergman M, Pirani CL. Nephrotic syndrome and immune complex glomerulonephritis associated with chlorpropamide therapy. Am J Med 1983 74(2) 337-42. 

Hebert LA, Birmingham DJ, Shen XP, Cosio FG, Fryczkowski A. Rate of antigen entry into the circulation in experimental versus naturally occurring immune complex glomerulonephritis. J Am Soc Nephrol 1994 5 S70-5. 

Thaiss et al. (1989) evaluated the effect of the immunosuppressant cyclosporin A on an active model of in situ immune complex glomerulonephritis. Wistar rats were preimmunized with human IgG and 2weeks after the last antigen injection, the left kidney was perfused with cationized human IgG in order to induce unilateral in situ immune complex glomerulonephritis. 

Adverse effects are in general uncommon, apart from allergy (above). It is salutary to reflect that the first clinically useful true antibiotic (1942) is still in use and is also amongst the least toxic. Only in patients with bacterial endocarditis, where the requirement for high doses can co-exist with reduced clearance due to immune complex glomerulonephritis, does a risk of dose related toxicity (convulsions) arise. 

Papayianni A, Serhan CN, Phillips ML, Rennke HG, Brady HR (1995) Transcellular biosynthesis of Upoxin A4 during adhesion of platelets and neutrophils in experimental immune complex glomerulonephritis. Kidney Int 47 1295-1302... 

Due to their inhibitory effects on DNA methylation, procainamide and hydralazine can induce autoreactive T cells by upregulating the expression of lymphocyte function-associated antigen-1 (LFA-1), which causes the cells to proliferate in response to normally subthreshold stimuli, including self (Yung et al. 1995). As a result, the adoptive transfer of T cells modified by in vitro treatment with procainamide or hydralazine induces an autoimmune disorder characterized by antinuclear antibodies (ANAs) and immune complex glomerulonephritis in naive mice (Quddus et al. 1993). 

One of the most important characteristics of this model is that oral dosing with D-pen induces autoimmune disease, thereby mimicking what occurs clinically. The clinical manifestations are also similar to those observed in humans specifically, both diseases are characterized by the production of ANAs, immune-complex glomerulonephritis, dermatitis, and arthralgia (Donker et al. 1984 Enzenauer et al. 1990). Another unique feature of this model is that the disease is idiosyncratic... 

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